Treatment toward a Cure: A Paradigm Shift in the Treatment of Diabetic and other Neuropathies
In the United States and most developed countries, the quality of medical care continues to grow in the treatment of acute disease and many cancers. Sadly, such has not been the case of many of chronic diseases. Efforts have largely been in management of symptoms rather than reversal or even cure. Diabetes, diabetic neuropathies and other neuropathy associated disease states consume large portions of healthcare resources in the United States and throughout the world.
By and large to date, care has only focused on symptom control and slowing the disease progression. At this time, there is no real effective treatment, only symptom management. We have developed a protocol for which compelling evidence exists that the clinical course of diabetic and other neuropathies is actually arrested and likely reversed.
To this end, we utilize advanced electronic signaling treatment (EST) to signal cell healing rather than smothering nerve and muscle cells with pharmacological agents. We also discovered these energy medicine techniques are practically devoid of side effects.
Peripheral neuropathy occurs as a component of several common and many rare diseases. It is heterogeneous in etiology, diverse in pathology and varied in severity. Peripheral neuropathy of the extremities is often undervalued as a significant problem worldwide, especially in the United States.
Neuropathy from diabetes and other causes is rampant in the United States. (>8 percent of the population by some estimates), and is projected to worsen. Neuropathy, at least subclinically, is often the first sign of diabetes; other end organ damage is less perceivable.
Morbidity associated with neuropathy from diabetic and other diseases are a major reason why patients seek medical care and are a huge cost to thirdparty payers, and the United States — and global communities — as a whole. This nerve disease affects millions worldwide by causing multiple foot, ankle, hand, wrist, as well as other muscular and skeletal disorders.
Components of Diabetic Peripheral Neuropathy
Diabetic peripheral neuropathy (DPN) is a particularly debilitating complication of diabetes mellitus and accounts for significant morbidity by predisposing the foot to ulceration and lower extremity amputation. It is estimated that between 12 percent and 50 percent of people with diabetes have some degree of DPN, which may be asymptomatic or symptomatic.
Symptoms may be disabling and may be manifested as both “negative” and “positive.” These symptoms include tingling, prickling, pins and needles, numbness, and pain (e.g., burning, lancinating, throbbing, stabbing, aching), along with allodynia (other pain or unusual sensation) and loss of proprioception (balance).
A predominant feature of DPN is sensory loss, but it is believed that all causes of peripheral neuropathy have a sensory, motor and autonomic neuropathy component. Sensory neuropathy causes paresthesia and loss of protective sensations, which can lead to sleep deprivation, ulcerations and lower extremity amputations.
Motor neuropathy causes imbalance leading to injuries and fractures, some forcing the patients to lose their independence. Autonomic neuropathy can alter everyday body functions, such as blood pressure, heart rate, bowel and bladder emptying, digestion, and lead to skin ischemia and Charcot events.
The costs to the world economy are staggering. In the United States alone, the annual total direct medical and treatment cost of diabetes was estimated to be $44 billion in 1997, representing 5.8 percent of total personal healthcare expenditures during that year.
The management of DPN and its complications is likely to form a large proportion of this total expenditure because treatment is often resource-intensive and long-term. In 2001, the total annual cost of DPN and its complications in the United States was estimated to be between $4.6 and $13.7 billion for Type I and Type II Diabetes.
“In the United States alone, the annual total direct medical and treatment cost of diabetes was estimated to be $44 billion in 1997…”
Up to 27 percent of the direct medical cost of diabetes may be attributed to DPN. These staggering figures cover the annual cost of DPN only, which is believed to represent only 30-40 percent of the prevalence of overall peripheral neuropathy and, as such, 60-70 percent of all the causes of peripheral neuropathy are not related to diabetes.
Together, not only can diabetic and other causes of peripheral neuropathy lead to tremendous debilitating complications, such as amputations, pain, numbness, loss of balance, sleep, strength, quality and length of life, and poly-pharmacy use, but they also account for significant overall morbidity and healthcare costs.
Some studies have shown that the costs of caring for the diabetic patient with neuropathy can be as much as $7,000 more per year than caring for the diabetic patient without neuropathy. Sadly, most of this cost is directed to symptom management and control only.
Treatment Options for Peripheral Neuropathy
Diabetic neuropathy is known to develop well before the patient has any symptoms, since many early symptoms are “negative.” The literature states unequivocally that the sooner treatment can be initiated, the greater the chances of reversal of the symptoms. This is a disease of the circulation.
Microvascular circulatory deficiencies caused by errors in glucose metabolism have direct effects on circulation to the nerves. There is also direct effects on the nerves themselves. Pain signals, in turn, trigger secondary peripheral and central hyperalgesia (increased pain and sensation), which enhances the body’s response to the microvascular insult.
On a local level, micro-inflammation and edema around the nerves also contribute to neuropathy and diseases such as carpal tunnel syndrome and Morton’s Neuromas.
Several modalities are currently used to treat diabetic or peripheral neuropathy. Modifying risk factors by lifestyle changes, vitamins and supplements, physical medicine, topical medicinal treatments, prescribed oral medications, transcutaneous electrical nerve stimulation (TENS) units, monochromatic infrared light energy (MIRE), Anodyne®, Microvas®, and surgery have all been used to treat PN patients.
The most common approach is oral medications, which only “papers over” the symptoms. According to Berger, 53.9 percent of diabetic PN patients are treated with opioids; 39.7 percent with anti-inflammatory drugs; 21.1 percent with serotonin-selective reuptake inhibitors (SSRI), such as Cymbalta; 11.3 percent with tricyclic inhibitors (TCA), such as Nortryptilline; and 11.1 percent with anticonvulsants, such as Neurontin and Lyricax. Many researchers and clinicians have observed no rational reason to treat the neuropathic patient with opiates.
The safety and efficacy of these medications throughout the literature over the years is equivocal at best. These medications have drawbacks. Major adverse effects could include risk of renal impairment, GI bleeding, sedation, dizziness, confusion, short-term memory impairment, constipation, nausea, swelling and physical dependence. Almost some or all of these adverse effects including the staggering healthcare costs of iatrogenic complications are well-documented with long-term usage of many of these medications.
Recently, further studies and sub-analysis performed have shown no statistical quality or merit in treatment modalities, such as TENS, MIRE, Anodyne®, Microvas® and even decompressive nerve surgery.
New Treatment for Peripheral Neuropathy
For the purposes of a discussion of pathophysiology, neuropathy from diabetes will be used as the model. We will discuss how chemistry and physics, both models that we, as humans, use to model these smooth-running biological systems, act together for healing. On a more basic level, we know that electrons (i.e. electron behaviors) tie together all of electrical and chemical medicine, and thus disease and curative medicine conceptually together.
Alternating current (AC) frequencies reverse and fire at a rate greater than a nerve (i.e., greater than 1,000 Hz). These depolarizing frequencies have been shown by Knedlitscheck et al. (1994) to stimulate utilization of cAMP.
It is well documented that cAMP directs all cell-specific activity, such as the repair of insulted tissue causing the metabolic cascade (leaking arachidonic acid) and decreasing level of noxious pain mediators (anti-inflammatory effect). The sustained depolarization of the cell increases intercellular levels and utilization of cAMP.
In fact, Kilgore and Bhadra (2004) have shown that nerve block via depolarization does occur at 2,000 to 20,000 Hz. Wali and Brain (1990) showed more sustained blockade. Wyss (1967, 1976) clearly showed that depolarization is sustained with the application of these currents, specifically 4,000 Hz.
New Treatment for Peripheral Neuropathy
A new, innovative and effective treatment has been established for diabetic and other peripheral neuropathies. This treatment is termed the Combination Electrochemical Treatment (CET), which incorporates two well-established procedures that have been combined into a protocol that shows great promise as a safe and effective treatment solution for diabetic, idiopathic and all other neuropathies.
CET consists of two procedures; an ankle block performed with local anesthetic, and Electronic Signal Treatment (EST), and is delivered by a unique sophisticated electromedical wave generator.
The peripheral nerve block injections are performed with a low volume and concentration of local anesthetic, and as such are not intended to produce the level of anesthesia required for performing surgery.
Bupivicaine is chosen because it does not fix to the tissues as rapidly; more time is available for the iontophoresis (electronic means of delivering a medication) of the local anesthetic into the tissues by EST.
No steroids are utilized at any time during this procedure. The blocks are aseptically performed utilizing Betadine; no infections have been reported in thousands of injections.
Electronic Signal Treatment
Electricity has been a powerful tool in medicine for thousands of years. All medical professionals are, to some degree, aware of electrotherapy. EST is a digitally produced alternating current, sinusoidal, electronic signal with associated harmonics that produce theoretically reasonable and/or scientifically documented physiological effects when applied to the human body. These signals are produced by advanced electronics not possible even 10-15 years ago.
EST medical device that delivers the electronic signals uses sophisticated communications-level technology to produce and deliver higher frequency signal energy in a continually varying sequential and random pattern via the specialty electrodes. This alternation of sequential and random signal delivery eliminates neuron accommodation.
Increasing blood flow: When mechanisms are considered, a note needs to be made about neuroanatomy. While myotomes and dermatomes have been well-documented in biomedical literature, as far as we can tell no such maps exist for the distal sympathetic C fibers anywhere in the body.
Still, we know enough about the C fibers to realize that these are primary in diabetes pathophysiology: these efferent fibers control the tone of local arterioles and, thus, are the critical contribution to the pathophysiology of small vascular structures and small nerve fibers (which are only viable as a function of these tiny arterioles).
Pathology in the small arterioles and nerve fibers combine to adversely affect the distal tissues of the legs (and later the hands).
CET has been shown to increase blood flow. The vasodilatation improves microcirculation, which has a salutary effect on the healing process in these oxygen-deprived nerve cells. The drainage function of the capillary system is improved as a result. Stimulation of motor nerve fibers results in excitation of the muscle fibers.
This has two effects on the blood flow: energy is used up, the metabolic rate is increased and blood flow is enhanced in the region of stimulating muscles. In addition, through the contraction activity of the muscle group, an active stimulation of the venous backflow occurs. Also, EST directly influences blood flow and lymph transport via sympathetic function imitation.
Anti-inflammatory action: EST, as an extension of presently available technology, also has potent anti-inflammatory effects. The potential long-lasting anti-inflammatory effects of some electrical currents are based on basic physical and biochemical facts, namely that of stimulating and signaling effective and long-lasting anti-inflammatory effects in nerve and muscle cells.
The safety of electrotherapeutic treatments in general and EST in particular has been established through extensive clinical use. EST utilizes computer-controlled, exogenously delivered specific parameter electroanalgesia using both varied amplitudes and frequencies of electronic signals.
“The goal of therapy during the treatment protocol is to reduce neuropathic symptoms including any pain, paresthesias, dysesthesias, allodynia and numbness.”
The electronic frequencies are programmed into the EST device and sequenced through a series of different complex waveforms. Each individual waveform represents a different mechanism of action. The electronic signals stimulate superior steroidogenic effects without the possible negative side effects of the injected steroid.
Blocking pain signals: Another primary action mechanism of EST is a reactive sustained depolarization of the nerve’s cell membrane. This occurs because multiple delivered signals fall within the absolute refractory period of the cell membrane. A pharmaceutical nerve block occurs when the Na channels are completely blocked, resulting in sustained hyperpolarization of the cell membrane.
EST produces a sustained depolarization of the cell membrane. All propagated pain and dysesthetic signals are blocked, but all cellular voltage-gated channels are allowed to function at optimum levels to their designated equilibrium point. Thus, metabolic activity of the cell is continued, the patient’s pain suppression is facilitated and all aspects of neuropathy can potentially be reversed.
More profound effects happen on a cellular level: the sustained depolarization that occurs has a direct effect to produce an electrical conformational change of the cell
membrane and activation of adenylyl cyclase, which converts ATP to cAMP. The positive affects of cAMP were discussed previously. Stimulation also activates the release of painsuppressing neuro-modulators found in the central nervous system (e.g. endorphin, encephalin and GABA).
Therapeutic Injections and EST Series
The first author, a board-certified anesthesiologist, interventional pain medicine specialist and Fellow of Interventional Pain Practice (FIPP) of the World Institute of Pain, has been using this block for more than five years. He introduced the CET concept to the International Spine Intervention Society at its annual convention in July 2008.
Diabetic peripheral neuropathy (DPN) and peripheral neuropathy (PN) patients have shown marked symptom reduction and motor function improvement with application of the CET. It is the authors’ position that nerve regeneration is really occurring.
Clinical objective human data of nerve regeneration from neuropathy patients in the authors clinics and the clinics of others have included changes in epidermal nerve fiber testing (ENFD), Neuralscan neurodiagnostic testing and nerve conduction velocity (NCV) testing.
Examples will be presented by the authors at the 6th World Medical Tourism& Global Healthcare Congress, in Las Vegas, in November 2013.
Clinically, the highest improvement in symptomology (reversal of pain, restoration of sensation and feeling to the extremities, increase strength, balance and quality of life) has been obtained with patients treated between 8-16 weeks. The treatment course is variable depending on the severity of the patient’s neuropathy and overall compliance to the treatment regimen.
The goal of therapy during the treatment protocol is to reduce neuropathic symptoms including any pain, paresthesias, dysesthesias, allodynia and numbness. Long-term goals include prevention of infections, amputations, misuse of medications, improvement of balance, sleep, overall function and quality of life, all of which have been accomplished in more than 80 percent of patients.
Summary and Conclusion
The clinical experiences of multiple MDs and DPMs have shown that the application of EST, when combined with the low-dose local anesthetic, favorably influences the peripheral vasculature and promotes nerve and cell regeneration. Many forms of neuropathy can be reversed over time with this effective, new treatment.
Our clinicians are seeing the nerve regenerative and growth capabilities of this treatment consistent with the above results. Little or no return of neuropathy symptoms from long-term post CET treatment has been observed. Our current patient treatment success, response rates and lack of relapse are substantial, along with three different kinds of objective proof of neural regeneration.
Further basic science studies regarding the exact mechanisms and clinical studies which would correlate risk factors, such as length of time prior to treatment, could yield even more effective protocols. Finally, Neuralscan testing of populations at risk for diabetic and other neuropathies could be an effective screening technique where early intervention may not require the 2-3 months in the current protocol.
About the Author
Robert H. Odell, Jr., is president and CEO of The Neuropathy and Pain Centers of Las Vegas. As a fellow of the Medical Scientist Training Program, he received his Ph.D. in Biomedical Engineering from Stanford University, in 1974, and his M.D. from Stanford in 1976. He completed his residency in anesthesiology at UCLA, and served as chief resident at Harbor/UCLA Medical Center, in 1982. He is a diplomate of the American Board of Anesthesiology (1983), American Academy of Pain Management (2001) and the American Board of Pain Medicine (2007) and a Fellow of Interventional Pain Practice (2008).
During the last several years, Dr. Odell has been working with some advanced electromedical devices which produce salutary effects for some of the most refractory pain management challenges. Research utilizes the Combined Electrochemical Treatment (CET), which combines the clinical benefits of these Electronic Signal Treatment (EST) devices with interventional pain management techniques to produce dramatic patient outcomes in a wide variety of refractory neuropathic pain states including low back pain, diabetic neuropathy, idiopathic neuropathy, failed spine fusion syndrome and carpal tunnel syndrome.
He has been practicing anesthesiology since the early 1980s, and pain management since 2001. He was instrumental in the development of a neurodiagnostic test used in his clinic to detect the spinal level of the pain generator in neck and low back pain, and now it is being utilized to test for neuropathy. He has extensive experience with a wide variety of non-interventional and interventional acute and chronic pain management techniques including vertebral axial decompression and electroanalgesia. Dr. Odell is a member of the International Spinal Intervention Society (ISIS), American Society of Anesthesiologists, and the American Society of Regional Anesthesia and Pain Medicine.